Analyzing Blood Pressure Ascent during Aging in Non-Diabetics: Focusing on Links to Insulin Resistance and Body Fat Mass.

Abstract

Background: A gradual upward progression of blood pressure (BP) occurs regularly in most humans during aging. This is unfortunate, because it is generally recognized that elevation of BP, even when relatively mild, is eventually detrimental to human health. Accordingly, considerably more understanding of the pathophysiology behind such a phenomenon is important in order to institute the correct remedies. Two components of the ubiquitous metabolic syndrome (MS) with nutritional implications, elevated insulin resistance (IR) and excess body fat mass (FM), are often postulated to be critical driving forces behind the elevated BP that is common with aging. The current study, therefore, focuses on the presence and importance of IR and/or body FM in BP regulation of non-diabetics over the lifespan.

Methodology: In cross sectional analyses, baseline data obtained from healthy, non-diabetic volunteers involved in prior clinical studies were analyzed by examining links between FBG measurements used as a surrogate for IR and body FM through their individual and combined effects on BP.

Results: A significant positive correlation was found between FBG and FM and also between each employed individually as independent variables to the dependent BP and heart rate (HR) variables. In volunteers with higher body FM compared to lower, average systolic BP (SBP) values are increased to some extent at the same FBG measurement suggesting that other factors related to FM in addition to IR are the basis for slight pressure differences. Considering quartiles based upon levels of FM and FBG, low FM-low FBG display significantly reduced average SBP, diastolic blood pressure (DBP), and HR compared to the upper FM-FBG quartiles. While readings of FBG and FM display a decline in elderly subjects after age 70 years (aging paradox), such does not occur with SBP.

Conclusions: IR is a major driving force behind BP regulation even in non-diabetics. FM influences BP substantially through its relationship with IR and also via other mechanisms directly linked to FM.